Oxidative stress, HDL and atherosclerosis
Нема приказа
Аутори
Vekić, JelenaKotur-Stevuljević, Jelena
Zeljković, Aleksandra
Stefanović, Aleksandra
Bogavac-Stanojević, Nataša
Vujović, Ana
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Oxidative stress is a result of an imbalanced equilibrium between reactive oxygen species (ROS) generation and their elimination by antioxidants. There is substantial evidence indicating that exacerbated oxidative stress is relevant for the development of atherosclerosis and its associated complications, especially cardiovascular disease (CVD). According to the oxidative modification hypothesis, oxidised low density lipoproteins (LDL) induce atherosclerosis by triggering an inflammatory cascade within the vascular wall. This process can be inhibited or delayed by the antioxidative and anti-inflammatory actions of high density lipoproteins (HDL). Clearly, paraoxonase-1 (PON1) is one of the most important contributors to the antioxidative capacity of HDL. Atherogenic dyslipidemia, oxidative stress and inflammatory conditions induce dramatic changes in HDL composition that considerably alters or attenuates HDL's anti-atherogenic effects. Such impairment of HDL's functions provides an impo...rtant link between oxidative stress and inflammation in the pathogenesis of atherosclerosis. This review summarises and discusses the possible synergistic effects of dyslipidemia, oxidative stress and inflammation in promoting atherosclerosis and its complications, as well as potential benefits of therapeutic modulation of HDL's atheroprotective activity.
Кључне речи:
Atherosclerosis / Cardiovascular disease / Diabetes / HDL / Inflammation / Oxidative stress / ParaoxonaseИзвор:
Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry, 2008, 7, 3, 158-165Институција/група
PharmacyTY - JOUR AU - Vekić, Jelena AU - Kotur-Stevuljević, Jelena AU - Zeljković, Aleksandra AU - Stefanović, Aleksandra AU - Bogavac-Stanojević, Nataša AU - Vujović, Ana PY - 2008 UR - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1139 AB - Oxidative stress is a result of an imbalanced equilibrium between reactive oxygen species (ROS) generation and their elimination by antioxidants. There is substantial evidence indicating that exacerbated oxidative stress is relevant for the development of atherosclerosis and its associated complications, especially cardiovascular disease (CVD). According to the oxidative modification hypothesis, oxidised low density lipoproteins (LDL) induce atherosclerosis by triggering an inflammatory cascade within the vascular wall. This process can be inhibited or delayed by the antioxidative and anti-inflammatory actions of high density lipoproteins (HDL). Clearly, paraoxonase-1 (PON1) is one of the most important contributors to the antioxidative capacity of HDL. Atherogenic dyslipidemia, oxidative stress and inflammatory conditions induce dramatic changes in HDL composition that considerably alters or attenuates HDL's anti-atherogenic effects. Such impairment of HDL's functions provides an important link between oxidative stress and inflammation in the pathogenesis of atherosclerosis. This review summarises and discusses the possible synergistic effects of dyslipidemia, oxidative stress and inflammation in promoting atherosclerosis and its complications, as well as potential benefits of therapeutic modulation of HDL's atheroprotective activity. T2 - Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry T1 - Oxidative stress, HDL and atherosclerosis VL - 7 IS - 3 SP - 158 EP - 165 DO - 10.2174/187152308785699281 ER -
@article{ author = "Vekić, Jelena and Kotur-Stevuljević, Jelena and Zeljković, Aleksandra and Stefanović, Aleksandra and Bogavac-Stanojević, Nataša and Vujović, Ana", year = "2008", abstract = "Oxidative stress is a result of an imbalanced equilibrium between reactive oxygen species (ROS) generation and their elimination by antioxidants. There is substantial evidence indicating that exacerbated oxidative stress is relevant for the development of atherosclerosis and its associated complications, especially cardiovascular disease (CVD). According to the oxidative modification hypothesis, oxidised low density lipoproteins (LDL) induce atherosclerosis by triggering an inflammatory cascade within the vascular wall. This process can be inhibited or delayed by the antioxidative and anti-inflammatory actions of high density lipoproteins (HDL). Clearly, paraoxonase-1 (PON1) is one of the most important contributors to the antioxidative capacity of HDL. Atherogenic dyslipidemia, oxidative stress and inflammatory conditions induce dramatic changes in HDL composition that considerably alters or attenuates HDL's anti-atherogenic effects. Such impairment of HDL's functions provides an important link between oxidative stress and inflammation in the pathogenesis of atherosclerosis. This review summarises and discusses the possible synergistic effects of dyslipidemia, oxidative stress and inflammation in promoting atherosclerosis and its complications, as well as potential benefits of therapeutic modulation of HDL's atheroprotective activity.", journal = "Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry", title = "Oxidative stress, HDL and atherosclerosis", volume = "7", number = "3", pages = "158-165", doi = "10.2174/187152308785699281" }
Vekić, J., Kotur-Stevuljević, J., Zeljković, A., Stefanović, A., Bogavac-Stanojević, N.,& Vujović, A.. (2008). Oxidative stress, HDL and atherosclerosis. in Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry, 7(3), 158-165. https://doi.org/10.2174/187152308785699281
Vekić J, Kotur-Stevuljević J, Zeljković A, Stefanović A, Bogavac-Stanojević N, Vujović A. Oxidative stress, HDL and atherosclerosis. in Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry. 2008;7(3):158-165. doi:10.2174/187152308785699281 .
Vekić, Jelena, Kotur-Stevuljević, Jelena, Zeljković, Aleksandra, Stefanović, Aleksandra, Bogavac-Stanojević, Nataša, Vujović, Ana, "Oxidative stress, HDL and atherosclerosis" in Anti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistry, 7, no. 3 (2008):158-165, https://doi.org/10.2174/187152308785699281 . .